Since their first use fifty years ago, chronic implantable electrodes have become a critical tool for exploring the function of neural tissue. In fact, chronic electrode recordings have contributed to the basic understanding of how neural networks process sensory stimuli and impart motor control. Moreover, these same electrodes can be used to actively stimulate regions of the brain, as well as to mimic natural sensory input and to initiate physical responses.
The ability to interface directly with the brain is making it possible for the blind to see, the deaf to hear, and the paralyzed to move. However, while great strides have been made in neural interfacial technologies, signal degradation due glial scar formation still limits the functional lifespan of chronically implanted electrodes.
The continued presence of an implanted electrode initiates a chronic foreign body reaction. Over time, the body isolates to the probe; activated astrocytes and microglia encapsulate the electrode, effectively displacing local neurons, hindering diffusion, and increasing interfacial impedance. Micromotion of the probe relative to surrounding tissue exacerbates this phenomenon, enhancing scar tissue formation in high stress areas.
One of the fundamental problems with current electrodes is the dichotomy between the material properties needed for implantation and the properties required to minimize long term neural trauma. Current microelectrodes must be stiff enough to retain their shape under the compressive load needed to drive them through neural tissue. Silicon microelectrodes possess the required stiffness but sacrifice flexibility. Moreover, the large mismatch between the modulus of silicon based probes (˜172 GPa) and the brain (˜0.1 MPa) has been identified as a contributing factor in glial scar formation and subsequent long term signal degradation. Efforts have been made to reduce scarring by developing coatings which improve neural cell attachment and growth and prevent astrocyte adhesion. However, such measures fail to address the severe mechanical mismatch between neural tissue and the probes themselves.
A number of relatively flexible probes have been developed to reduce micromotion-induced tissue strain. Such devices are typically fabricated from polymers such as polyimide using Bio-MEMS techniques, and have elastic moduli of ˜2 GPa. Implantation using traditional techniques is difficult due to their increased flexibility. Previous approaches have attempted to address this issue by creating an incision in the pia prior to insertion and/or creating a shape memory probe that slowly exerts force on neural tissue, allowing for gradual plastic deformation of the tissues surrounding the device. Still other approaches have developed techniques for polymerizing flexible conductive poly(3,4-ethylenedioxythiophene) in direct contact with living neural tissue, stiffened polymeric probes by means of fluid filled channels, bonded stiff metallic elements to the polymer and/or used ridged structures to penetrate the tissue, leaving the flexible probe behind after withdrawal. Despite using soft materials, the majority of such devices must compromise flexibly for the ability to exert enough compressive force for implantation.